Implantable medical devices (IMDs) that generate and apply to excitable muscle tissue, nerves, and organs in the pelvic region to treat pelvic floor disorders are clinically available or have been proposed. Pelvic floor disorders include urinary and fecal incontinence, erectile dysfunction, and pelvic pain.
As set forth in U.S. Pat. No. 6,964,699, urinary incontinence is a significant clinical problem and a major source of disability and dependency. The most frequently occurring types of urinary incontinence are stress incontinence, urge incontinence, overflow incontinence, and mixed incontinence characterized by involuntary loss of urine, beyond the individual's control, due to the loss or diminution of the ability to maintain the urethral sphincter closed as the bladder fills with urine. Muscles involved in controlling the urinary flow include primarily the urethral sphincter and the levator ani, with the cooperation of fibromuscular extensions along the urethra and other muscles in the general region of the pelvic diaphragm.
Fecal incontinence is a condition characterized by involuntary defecation or passage of feces through the anal canal due to injury to or weakness of one or more of the internal anal sphincter, the external anal sphincter, and the levator ani.
As set forth in U.S. Pat. No. 6,896,651, male or female stress urinary incontinence (SUI) occurs and results from weakness or inability of pelvic muscles to hold back urinary flow from the bladder when abdominal pressure increases due to common physical or emotional stress events, such as coughing, laughing or mild physical exertion. Stress incontinence is typically associated with either or both of urethral hypermobility and intrinsic sphincter deficiency. Urethral hypermobility is characterized by weakness of or injury to pelvic floor muscles that causes the bladder to descend during abdominal straining or pressure, allowing urine to leak out of the bladder. Intrinsic sphincter deficiency is characterized by the inability of the urethral musculature to completely close the urethra or keep it closed during stress.
In urge incontinence, a sudden, urgent need to pass urine causes involuntary urination, before the patient can get to a toilet. The condition may be caused by damage to nerve pathways from the brain to the bladder or by psychosomatic factors, leading to involuntary bladder contraction. Overflow incontinence occurs when the bladder is unable to empty normally. Weak bladder muscles, caused e.g. by nerve damage from diabetes, or a blocked urethra, caused e.g. by tumors or urinary stones, are among the more common causes of overflow incontinence. Frequency or urgency involves the need or urge to urinate on an excessively frequent or habitual basis. Some patients exhibit combinations of these types of incontinence that are often called mixed incontinence.
Many options are available to treat incontinence in its various forms, including Kegel exercises, biofeedback, timed voiding or bladder training, medications, pessaries, invasive or minimally invasive surgery, catheterization, and implantation IMDs. Urinary incontinence IMDs are typically implanted in relation to the tissue structure around the urethra including the urethral wall, the bladder neck, bladder suspension ligaments, the urethral sphincter, pelvic ligaments, pelvic floor muscles, fascia, and the like. Urinary incontinence IMDs include urethral tapes or slings that support the urethra, prosthetic sphincter systems that compress the urethra until voiding is initiated, and periurethral or transurethral injection of a mass of biocompatible bulk-enhancing or bulking agent or an inflatable balloon into the tissue structure around the urethra.
Male and female urethral sling procedures are disclosed in commonly assigned U.S. Pat. Nos. 6,382,214 and 6,652,450, for example, and further female urethral sling procedures are described in commonly assigned U.S. Pat. Nos. 6,641,524 and 6,612,977, and in U.S. Patent Application Publication Nos. 2002/0165566 and 2005/0245787, for example, and publications and patents cited therein. The implantation of certain urethral slings involves the use of delivery systems configured for and techniques that involve transvaginal, transobturator, supra-pubic and pre-pubic exposures or pathways.
In surgical approaches disclosed, for example, in commonly assigned U.S. Patent Application Publication Nos. 2005/0043580 and 2005/0065395, elongated self-fixating urethral slings are implanted for treating female prolapse employing a pair of sling implantation instruments or tools. The sling implantation tools comprise a handle with an elongated needle portion terminating in a needle distal end adapted to be coupled to free ends of the urethral sling and have mirror image right and left handed needle shapes.
The sling implantation tools disclosed in the above-referenced 2005/0043580 publication have a curvature in a single plane and correspond generally to the BioArc™ SP and SPARC™ single use sling implantation tools sold by American Medical Systems, Inc., (Minnetonka, Minn.) in a kit with an elongated urethral sling. The sling implantation tools disclosed in the above-referenced 2005/00653985 publication have a curvature in 3-dimensional space and correspond generally to the BioArc™ TO and MONARC™ TO single use sling implantation tools sold by American Medical Systems, Inc., in a kit with an elongated urethral sling. In each such sling implantation tool, the needle portion has a proximal straight portion extending from the handle and a distal shaped portion terminating in a needle distal end. The needle portion is sized and shaped so that the distal end may initially be moved through an abdominal incision and advanced posterior to one of the right and left posterior ischiopubic pubic ramus of the pelvic girdle spaced from the bladder to a urethral incision accessing the urethral tissue structure, e.g., a vaginal incision in the region of the vaginal apex of a female patient.
The needles of the BioArc™ TO and MONARC™ TO implantation tools are curved in three-dimensional space so that the needle tip may be advanced toward and through the obturator membrane of the obturator foramen, and then toward a vaginal incision in the region of the vaginal apex. The surgeon employs a learned wrist motion of the hand grasping the handle and pressure feedback felt through the handle to guide advancement. Also, the surgeon may palpate the vaginal wall with the fingers of the free hand to locate the needle tip and guide it toward and through the vaginal incision to expose the needle tip. The procedure is repeated using the other of the right and left hand sling implantation tools to advance the needle tip through a second skin incision and the other of the respective right and left obturator membranes to expose both needle tips through vaginal incisions.
In the above-referenced U.S. Patent Application Publication No. 2002/0165566, a curved needle is provided having a detachable handle for making a similar tissue pathway by extending the needle end through the vaginal incision, through the tissue, and then out an abdominal skin incision. The handle is detached, and the sling end coupled to the needle end extending from the vaginal incision. The needle end extending from the abdominal skin incision is then grasped to pull the sling through the tissue pathway so that the sling end can be detached from the needle end outside the abdominal incision.
Returning to the use of the BioArc™ TO and MONARC™ TO implantation tools, right and left subcutaneous transobturator pathways are formed through the right and left obturator foramen and connective tissue attached to the right and left posterior ischiopubic pubic ramus of the pelvic girdle. This procedure is preformed without visualization of the needle tip, and care must be taken to avoid deviating posteriorly and penetrating the bladder and to otherwise avoid damaging any of the obturator nerves, the superficial epigastric vessel, the inferior epigastric vessel, the external iliac artery and the internal iliac artery.
The free ends of the elongated urethral slings are implanted through the tissue pathways employing the right handed and left handed sling implantation tools as further described in the above-referenced U.S. Patent Application Publication Nos. 2005/0043580 and 2005/0065395. Generally speaking, the free ends of the elongated urethral slings are coupled to the needle distal ends, and portions of the sling are drawn through the pathways to draw a central sling portion against the urethra to provide support. The free ends of the elongated urethral slings include dilating connectors for connecting with the needle distal ends so that the pathways are dilated as the connectors are drawn through them. The dilating connectors are drawn out through the abdominal skin incisions and are severed from the urethral sling. The urethral sling portions other than the central portion may be covered with a detachable protective film sheath that is then withdrawn exposing mesh that is sutured to subcutaneous tissue layers. Chronic tissue ingrowth into the mesh pores stabilizes the urethral sling. A similar procedure creating a tissue pathway from a urethral incision accessing the urethral tissue structure and an abdominal skin incision may be followed to install an elongated urethral sling to support the male urethra to alleviate incontinence as described in regard to certain embodiments in the above-referenced '450 patent.
In another approach, a neuromodulator or neurostimulator implantable medical device (IMD) is implanted in a patient's body to electrically stimulate nerves controlling external sphincter and bladder functions, e.g., the sacral nerves in the nerve root or at the peripheral sciatic nerve or the pudendal nerve. In still another approach a muscle tissue stimulator IMD is implanted in a patient's body to directly electrically excitable muscle tissue of a sphincter, e.g., tissue structure around the urethra or anus. The IMD in either case comprises a medical electrical lead, also known as a neural lead or tissue stimulation lead, and an implantable pulse generator (IPG).
According to several known surgical treatment methods for implanting a neurostimulator IMD to stimulate a nerve, one or more nerve stimulation or neural stimulation electrode supported at the distal end of a neural lead is disposed at a nerve stimulation site. It is typically necessary to employ introducers and stiffening stylets and/or guidewires to position the distal neural stimulation electrode(s) in operative relation to a nerve at the target stimulation site. A proximal lead connector assembly is coupled to a connector header of the IPG, so that the IPG and neural lead comprise the neurostimulator IMD. See for example, U.S. Pat. Nos. 5,569,351, 4,607,639, 4,739,764, 4,771,779, and 6,055,456 regarding electrical stimulation of the sacral nerve to control bladder function. The InterStim® System for Urinary Control sold by Medtronic, Inc., Fridley, Minn., comprises such an IPG, which is surgically implanted in the lower abdomen, and a medical electrical lead that extends from a connection with the IPG to exposed neural stimulation electrodes disposed adjacent the sacral nerve near the sacrum (the bone at the base of the spine) in a major surgical procedure—sometimes six hours under general anesthesia. The IPG continuously generates electrical stimulation pulses that are applied to the sacral nerve to control urinary voiding. The continuous electrical stimulation of the nerve has been found to control urge incontinence in some patients.
Stimulation of the pudendal nerve employing a neurostimulator IMD as an alternative to sacral nerve stimulation has long been proposed. Electrical stimulation delivered by an intravaginal or a perineal surface electrode has been shown to inhibit premature and inappropriate detrusor contractions. The mechanism for such effects appears to derive from the electrical stimulation of pudendal nerve afferents (sensory receptors or sensory nerve fibers). Input into the pudendal afferent system inhibits a parasympathetic reflex loop consisting of bladder wall afferents (sensory reflexes) and efferents (motor reflexes). This parasympathetic loop normally senses a distension of the bladder via the afferent limb and responds by sending an efferent signal to contract the bladder. Although such stimulation has shown therapeutic effects, electrode placement and on-going stimulation do not lend themselves easily to chronic stimulation.
Stimulation of the tissue structure around the urethra is also proposed in the above-referenced '651 patent, in U.S. Pat. No. 6,862,480, and in Application Publication No. 2005/0216069, all assigned to Biocontrol Medical, Ltd., to treat both urinary stress incontinence and urge incontinence. The tissue stimulator IMD comprises a control unit or IPG coupled through medical electrical leads to one or more sense/stimulation electrodes and to one or more mechanical sensor. The IPG is preferably implanted under the skin of the abdomen or genital region, the sense/stimulation electrodes are preferably implanted in the pelvic region so as to be in electrical contact with one or more of the muscles that regulate urine flow from the bladder, e.g., the urethral sphincter and the levator ani, and the mechanical sensors are preferably implanted on, in or in the vicinity of the bladder. The sense/stimulation electrodes are described as flexible wire, intramuscular-type, electrodes, about 1-5 mm long and 50-100 microns in diameter, and may be formed in the shape of a spiral or hook, so that the shape facilitates fixation in tissue. The mechanical sensors supported on a sensor lead body comprise one or more pressure, force, motion or acceleration sensor, or an ultrasound transducer, that generate signals responsive to motion, to intravesical or abdominal pressure, or to urine volume in the bladder, and are thus indicative of possible imminent incontinence.
The IPG receives and processes electromyographic (EMG) signals sensed across the electrodes and the mechanical sensor output signal to distinguish between EMG signals indicative of urge incontinence, EMG signals indicative of stress incontinence, and EMG signals that are not due to incontinence. Electrical stimulation having stimulation parameters tailored to inhibit urge incontinence are generated by the IPG and delivered across the electrodes when the sensed signals are indicative of impending urge incontinence. Similarly, electrical stimulation having stimulation parameters tailored to inhibit stress incontinence are generated by the IPG and delivered across the electrodes when the sensed signals are indicative of impending stress incontinence. Certain implantation methods for implanting the tissue stimulation IPG in the body of a female patient are described in the '651 and '480 patents. It is suggested that similar methods would be employed in the implantation of the IMD in a male patient.
In one method, a subcutaneous surgical pocket is made to receive the IPG approximately 1 cm cephalad to the pubic bone. A vaginal mucosa incision is made at a site approximately 0.5-1 cm anterior and lateral to the urethral meatus. A subcutaneous pathway is tunneled between the pocket and the vaginal mucosa incision, and the lead body is extended through the pathway to dispose a distal portion of the lead outside the vaginal mucosa incision. A 5 French, splittable short introducer is inserted into the vaginal mucosa incision adjacent to the lead and advanced with care slightly medially, i.e., towards the urethra, about 2.5 cm, to a site 0.5-1 cm lateral to the urethral wall. The distal end of the stimulation lead is inserted and advanced through the lumen of the short introducer into the urethral sphincter. The introducer sleeve is split apart to withdraw it over the lead body after the stimulation electrode is properly positioned. The stimulation lead body is sutured to the subcutaneous tissue to secure it from movement. The exposed distal portion of the lead body is retracted subcutaneously, and the vaginal mucosa incision is closed.
To implant the sensor lead, an 8 French introducer is inserted through the pocket incision, between the fascia and muscle tissue, and advanced into the retropubic space. The sensor lead bearing a distal pressure or electrical sensor is stiffened by a stiffening stylet and the lead body is advanced through the introducer to dispose the sensor at a desired position, e.g., in the retropubic space or between fascia and muscle. The sensor lead body is also sutured to the fascia, the stylet is withdrawn, and the introducer is removed. The sensor lead and stimulation lead connectors are coupled to the IPG. The IPG is disposed in the pocket and the pocket is closed after testing the IMD to ascertain that all connections are secure and that sensing and stimulation can be reliably provided.
This method of positioning the stimulation electrodes in or proximate the urethral sphincter surrounding the urethra can be troublesome since there is a tendency that the stimulation electrode will be retracted when the introducer sleeve is split and withdrawn. In addition, the routing of the lead body through the subcutaneous pathway relative to the pubic bone can also stress the lead body and contribute to electrode dislodgement. Suturing the lead body to elastic tissue does not necessarily inhibit dislodgement. Moreover, care must be taken in placing sutures directly against a lead body to avoid damage to the insulating sheath or the conductors within the sheath. A suture sleeve may be employed, but it may be difficult to locate the relatively bulky sleeve in a place where suturing to tissue would be effective.
A wide variety of active (tissue penetrating) and passive (non-penetrating) fixation mechanisms have been proposed to retain cardiac pacing electrodes, cardioversion/defibrillation electrodes, brain stimulation electrodes, and neural stimulation electrodes at a selected stimulation site. Active fixation helical screws and hooks are not suitable for fixation to or about nerves due to the potential for nerve damage during implantation or due to micro-dislodgement in chronic implantation. A wide variety of passive fixation tines and shaped lead bodies are employed or proposed for sacral nerve and epidural space stimulation electrodes. It is also suggested that hook or spiral active fixation devices be incorporated at the distal ends of tissue stimulation leads disclosed in the above-referenced '651 and '480 patents and in Application Publication No. 2005/0216069. Unlike the myocardium of the heart, the tissue structure adjacent the urethra or anus is relatively soft, and hook or spiral active fixation devices do not hold as well as they do in the myocardium.
It is also suggested in U.S. Pat. No. 4,010,758 disclosing a pacing lead that a Dacron mesh suture pad surrounding an active fixation, helical, spiral-shaped electrode may promote tissue ingrowth chronically to augment the fixation achieved acutely. In use, the spiral-shaped electrode is screwed into the myocardium, and the mesh suture pad is sutured to the myocardium. Stomach wall stimulation leads are disclosed in U.S. Pat. No. 6,952,613 that employ similar helical and hook shaped active fixation mechanisms having such a Dacron mesh suture pad that is adapted to be sutured to the tissue.
It would be desirable to provide alternative fixation mechanisms to stabilize the distal tissue stimulation electrodes of tissue stimulation leads at stimulation sites in the pelvic region to treat selected pelvic disorders.